Too much sodium

Introduction to too much sodium Hypernatremia is also called hypernatremia, and serum sodium concentration >145mmol/L is hypernatremia. Hypernatremia is bound to have an increase in plasma osmotic pressure, so it is also called high-sodium hyperosmolar syndrome. Hypernatremia only reflects an increase in serum sodium concentration, and the total amount of sodium in the body can be increased, normal, or reduced. It is common in the clinical input of sodium chloride solution, mostly caused by increased extracellular fluid tissue edema, pulmonary edema and heart failure. basic knowledge The proportion of illness: 45% Susceptible people: no specific population Mode of infection: non-infectious Complications: hypernatremia

Excessive sodium cause

Insufficient water intake (25%):

Seen in the water source, stunned patients do not know how to drink water or help the water or disease caused by swallowing disorder. Stop the water (including water in the food). The loss of body fluid accounts for % of body weight. Completely water-d-the loss of body fluid reaches the body weight. % can cause death.

Excessive water loss (20%):

Common in diabetes insipidus osmotic diuretic diarrhea vomiting into the excessive urinary concentrating dysfunction and insufficient water supplement.

Sodium excretion disorder (25%):

Decreased sodium excretion in patients with adrenal hyperfunction is often accompanied by a decrease in sodium and sodium excretion. It is also seen in this patient's ability to release ADH and is barrier-free. The "osmotic pressure threshold" for releasing ADH is increased when the osmotic pressure in the body is increased to ADH is released when it is normal to a higher degree. It is called "idiopathic hypernatremia" clinically.

Too much sodium input (15%):

Commonly used in the injection of NaHCO3, excessive hyperosmotic NaCl input, etc., patients with more severe blood volume.

Excessive sodium prevention

Excessive sodium often occurs in other diseases, such as burns, head injury, COPD, liver transplantation, adrenal hyperfunction, etc. Therefore, in the treatment of these diseases, attention should be paid to prevent electrolyte imbalance, and patients with symptoms of this disease should be promptly performed. Treatment, to prevent further development and more serious diseases, once the high blood sodium is found in the early stage, all sodium-containing liquid should be immediately stopped, and the hypotonic liquid should be changed. If the person can not drink water, the stomach tube can be left and the temperature can be continuously dripped. Boiling water to relieve high blood sodium, and promote the discharge of sodium; actively control infection, cooling; blood glucose monitoring, actively control blood sugar to the normal range; after the edema period, if the condition allows, stop hypertonic diuretics, most patients The above treatment can obtain better effects and can effectively prevent further development of the disease.

Excessive sodium complications Complications, hypernatremia

Clinically, water and sodium balance disorders are often mixed, which may be sodium deficiency combined with water shortage or high sodium combined with excessive water; it may also be sodium deficiency combined with excessive water or high sodium combined with water shortage, so a comprehensive analysis of medical history, Clinical manifestations and laboratory test results, grasping the primary factors and major contradictions.

1. Diabetic patients with severe sodium infection caused by severe infection through diet control and oral hypoglycemic drugs, most patients can maintain normal blood sugar levels in normal times, once concurrent infection, prone to severe hyperglycemia and hypernatremia. The reasons for hyperglycemia are:

1 stress response, the levels of adrenal glucocorticoids, growth hormone, glucagon, etc. are significantly increased, and inhibition of the role of insulin treatment resulted in a significant increase in blood glucose.

2 tissue cells have decreased sensitivity to insulin.

3 catabolism enhanced, the synthesis of glycogen, the ability to lower blood sugar decreased.

4 Severely infected patients need adequate energy supply and no dietary restrictions. Patients can have severe hyperglycemia in a short period of time, but not necessarily ketoacidosis. Continued application of oral hypoglycemic agents and general insulin therapy can not be controlled. Significant hyperglycemia leads to a significant increase in plasma osmotic pressure, resulting in osmotic diuresis, loss of electrolytes less than the loss of water, resulting in concentrated hypernatremia, with a certain degree of sodium loss; patients with severe infections combined High fever and high catabolism, large loss of water in the respiratory tract and skin, further aggravating concentrated hypernatremia; diabetic patients are mostly elderly, diabetes and old age are easy to combine with the decline of renal tubular concentrating function, resulting in a further proportion of drainage Excessive sodium excretion, increased concentration of hypernatremia; anti-infection or hypoglycemia and other infusion treatment often intentionally or unintentionally input physiological saline or 5% glucose normal saline, resulting in the true increase of blood sodium. Due to blood concentration and renal blood flow reduction, patients with high chlorine, hyperkalemia and elevated urea nitrogen, the body found more obvious signs of dehydration.

(1) Principles of treatment: elevated blood glucose is the basis of hypernatremia, and blood concentration is the main cause of hypernatremia, and the input of sodium ions is often an important factor for further aggravation. Therefore, blood sugar should be controlled, the amount of fluid should be increased, and the input of sodium ions should be limited.

Hypernatremia

(2) Controlling blood sugar: Applying a larger dose of insulin, in order to control the rate of blood glucose decline, intravenous infusion should be used to avoid subcutaneous injection. In theory and habitually, physiological saline should be input, and after the blood sugar drops significantly, the 5% glucose solution is used. Need to pay attention to ensure that the blood glucose concentration gradually declines, if it can not effectively decline, with the input of physiological saline, it may further aggravate high sodium and hyperosmolaremia, if necessary, micro pump can be used, which can better control sodium chloride. The amount of input. Of course, the rate of decline in blood glucose concentration should not be too fast, otherwise it will lead to a rapid decrease in plasma osmotic pressure, a large amount of water entering the red blood cells to hemolyze, brain edema, and the risk of hypovolemic shock. After the blood glucose concentration drops to 8-12 mmol/L, it is considered to reach an appropriate level, which is not required and should not be lowered to a normal level.

(3) Increase the amount of fluid replacement: In patients with unstable blood pressure, the colloid should be entered at the same time; in patients with stable blood pressure, water intake and input should be increased rapidly. Commonly used intravenous rehydration is mostly 5% glucose solution and normal saline. It is difficult to control the input of sugar and sodium ions. Therefore, patients who are mainly ingested and who can enter the water independently can drink water by themselves; otherwise, they should be supplemented by gastric tube. Of course, hypotonic glucose and hypotonic sodium chloride solution can also be supplemented by intravenous.

(4) Controlling the amount of sodium ions: The above measures can better control the amount of sodium ions. However, with the control of blood sugar and the improvement of body fluid volume, the concentration of sodium, potassium and chloride ions may decrease. When the blood concentration of these ions reaches the normal low level, the supplement of sodium chloride and potassium chloride should be increased. Causes low sodium, low chlorine and hypokalemia.

(5) Check of blood sugar and electrolyte: It should be checked once every 2 hours, and the number of inspections should be reduced after the condition is stable.

2. Severe lung infection or acute lung injury complicated with hypernatremia patients with large loss of water in the respiratory tract and skin, easily lead to concentrated hypernatremia, patients with artificial airway to lose more water; anti-infective and other infusion therapy is also often Intentional or unintentional input of normal saline or 5% glucose normal saline, resulting in increased true serum sodium, so patients with mixed hypernatremia, should be a large amount of water, supplemented by gastrointestinal supplements. After the blood volume is improved, on the one hand, rehydration, on the one hand diuretic.

Symptoms of excessive sodium common symptoms nausea and vomiting hypokalemia irritability, uncomfortable coma, convulsions, loss of water, fever, nausea

Symptoms of this disease may include: fatigue, headache, irritability, etc., which may occur at an early stage, and then gradually progress to tremor, convulsions, and even coma and even death due to irreversible damage of brain tissue. Patients with intracranial hemorrhage may have Localization symptoms, neurological examination may appear hyperreflexia, neck stiffness, vertebral body bundle sign positive, etc. In many cases, lumbar puncture cerebrospinal fluid has red blood cells, increased protein, etc., other symptoms vary according to the basic lesions causing the disease, etc. If caused by diabetes insipidus, there is obvious polyuria, and those with excessive skin loss may have fever. If too much hypertonic NaCl or NaHCO3 is injected, there will be symptoms of heart failure such as high blood pressure, difficulty in breathing, and cough.

Hyperkalemia is mainly due to the hyperosmotic state caused by high blood sodium concentration, so that the water in the cells is precipitated, and the cells lose water, especially the brain cells lose water, which can cause a series of nervous system symptoms, the faster the disease, the symptoms The more obvious, like hyponatremia, the symptoms of slow-onset hypernatremia are generally relatively light, because brain cells can transfer extracellular Na+K+ into cells while at the same time synthesizing many small ones. Molecular permeable substances, mainly inositol, glutamic acid, and glutamine, which can participate in intracellular osmotic particle composition, thereby preventing excessive dysfunction of cells and causing dysfunction.

Excessive sodium check

For patients suspected of having too much sodium, the following tests should be performed:

(1) Physical examination The early prominent symptoms of hypernatremia are thirst. In severe cases, the brain cells are dehydrated and mainly manifest as symptoms of the nervous system, such as irritability, lethargy, hyperreflexia, increased muscle tone, and later convulsions and convulsions. In the examination of the body should pay attention to the patient's mental performance and symptoms of skin dehydration, with or without circulatory failure.

(2) Laboratory examination of blood sodium concentration is generally higher than 145 mmol / L, plasma osmotic pressure is also increased, daily urine volume urine and urine relative density determination, renal function test including urea nitrogen muscle with PSP And urine concentration and dilution test, etc., for patients with suspected diabetic primary aldosteronism Cushing syndrome to determine the endocrine function.

Sodium overdiagnosis

diagnosis

There are mainly the following characteristics in diagnosis:

1. History: Insufficient sodium chloride solution, especially when kidney function is low.

2. Clinical manifestations: mainly due to increased extracellular fluid, tissue edema, pulmonary edema and heart failure often occur.

3. Auxiliary examination: It can be found that the blood sodium content is elevated or normal.

Differential diagnosis

(1) Diabetes insipidus

Also known as pituitary diabetes insipidus, is the lack of ADH secretion in the posterior pituitary, the cause of the disease is unknown, the clinical features are polydipsia, polydipsia, polyuria (daily urine volume up to 5-10 L), low urine relative density (1.001 A 1.005), low urine osmotic pressure (50 ~ 200mmol / L), clinically divided into idiopathic diabetes insipidus and secondary diabetes insipidus, the latter is due to hypothalamic pituitary tumors, brain trauma, surgery, Inflammation is caused by the fact that when the lesion affects the thirst center of the hypothalamus and loses thirst, it is often unable to replenish water in time, resulting in severe dehydration or even death. When suspected diabetes insipidus, it should be tested by vasopressin and plasma ADH. To confirm the diagnosis, if necessary, head CT and X-ray examination should be performed to exclude pituitary tumors.

(two) renal diabetes insipidus

For hereditary diseases, the clinical manifestations are similar to those of diabetes insipidus. Most of the patients are boys. The disease occurs several months after birth. After the injection of vasopressin, the urine volume is not reduced, the urine specific gravity is not increased, and the plasma ADH concentration is significantly increased. Different from pituitary diabetes insipidus.

(3) Interstitial nephritis and severe renal dysfunction

Caused by a large number of causes, in addition to pyelonephritis, drugs (salt, demethyl chlortetracycline, etc.), low potassium, high calcium, urinary tract obstruction, gout, etc. can cause the disease, hypernatremia, polyuria, Dehydration can be differentiated according to medical history, renal function test and serum electrolyte measurement.

(4) Diabetic hyperosmolar coma

More common in elderly patients, mild diabetes before the onset of illness or even diabetes, often due to infection, the use of diuretics or glucocorticoids induced, clinical manifestations in addition to hypernatremia, dehydration is mainly neurological symptoms, such as not Clear, lethargy, hemiplegia, aphasia, convulsions, etc., easily confused with cerebrovascular accidents, this disease should be differentiated from hypernatremia caused by osmotic diuretics.

(5) Idiopathic hypernatremia

The cause is unknown, clinically rare, the diagnostic criteria are: 1 persistent hypernatremia; 2 no significant dehydration and thirst; 3 urine into hypertonic ban, indicating that the body still has the ability to secrete ADH; 4 kidney The small tube still responds to ADH. When vasopressin is applied, it can cause water retention. It is considered that this disease is the "threshold increase" of ADH release.

In addition, it should be differentiated from secretory diseases such as primary aldosteronism and hypercortisolism.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.